Sunday, December 19, 2010

Most people can count calories. Many have a clue about where fat lurks in their diets. However, fewer give carbohydrates much thought, or know why they should.

But a growing number of top nutritional scientists blame excessive carbohydrates — not fat — for America's ills. They say cutting carbohydrates is the key to reversing obesity, heart disease, Type 2 diabetes and hypertension.

"Fat is not the problem," says Dr. Walter Willett, chairman of the department of nutrition at the Harvard School of Public Health. "If Americans could eliminate sugary beverages, potatoes, white bread, pasta, white rice and sugary snacks, we would wipe out almost all the problems we have with weight and diabetes and other metabolic diseases."

It's a confusing message. For years we've been fed the line that eating fat would make us fat and lead to chronic illnesses. "Dietary fat used to be public enemy No. 1," says Dr. Edward Saltzman, associate professor of nutrition and medicine at Tufts University. "Now a growing and convincing body of science is pointing the finger at carbs, especially those containing refined flour and sugar."

High-fat (HF) diets of 2 weeks have been shown to accelerate gastric emptying (GE). To date, no studies have shown any alteration in GE following shorter HF diets. The aim of this study was to assess if an HF, high-energy diet of 3 days can adapt gastrointestinal (GI) transit, blood lipids and satiety.Subjects/Methods:

Eleven male volunteers participated in a study consisting of three, 3-day interventions each separated by a test day. During the first intervention, volunteers recorded their diet. In the second and third interventions, volunteers repeated their food diary plus either a low-fat yogurt or HF yogurt supplement in randomized order. Test days involved measurement of GE using the 13C octanoic-acid breath-test, mouth-to-caecum transit time (MCTT) using the inulin H2 breath test and satiety using visual analogue scales. Blood samples for measurement of lipaemia were taken using a venous cannula.Results:

MCTT was different between the three test days (P=0.038), with the shortest MCTT following the HF intervention. GE was shortest following the HF intervention. There were no differences in satiety between the interventions. The High Fat intervention reduced triglycerides, total cholesterol and low-density lipoprotein cholesterol, and increased high-density lipoprotein cholesterol.Conclusion:

This study shows that changes in GI transit owing to an HF diet can occur in a time period as short as 3 days.

AbstractObjective:To investigate associations between vascular risk profile and cerebral glucose metabolism.Methods:Subjects ranged from normal to having dementia (age >55 years) and underwent neuropsychological testing, MRI, and FDG PET scanning (n = 58). The Framingham Cardiovascular Risk Profile (FCRP) and its individual components were used as covariates in regression analyses with each PET scan using SPM2.Results:Analyses revealed broad areas of the frontal lobe in which higher FCRP was associated with lower normalized glucose metabolism including the superior medial frontal, superior frontal and superior orbital frontal cortex and the ventrolateral prefrontal cortex. Significant associations were predominately found in the left hemisphere. Independent component analyses revealed interesting regions but further confirm the relevance of the integrative measure of coronary risk.Conclusions:Although the mechanism of this association bears further investigation, this finding provides further evidence that vascular risk factors have malignant effects on the brain, particularly in the prefrontal cortex.Frontal lobe dysfunction is associated with attention deficit disorder. Not mentioned here, but these cardiac risk factors are also associated with depression, a condition known as vascular depression.

Friday, November 19, 2010

Unless you’ve been living in a cave for the past few months, you probably read “New Age Caveman in the City,” the New York Times feature on aspiring Stone Agers in NYC. If so, you may remember Melissa McEwen as the lone cavewoman of the group, providing some refreshing gender balance to the paleo diet argument that rice cakes and rolled oats aren’t health foods — meat is.

Melissa discusses the paleo diet and all its meaty nutrients on her site Hunt.Gather.Love, on Twitter and sometimes in the comments of the blog you’re reading right now. On top of that, she’s scheduled to speak at the Ancestral Health Symposium in Los Angeles next summer and she’s just been interviewed by Let Them Eat Meat. You might say that Melissa is already a star in the paleo world.

But of course none of this would have been possible if Melissa had stuck with veganism.

Melissa holds building together

What’s all this about animal foods being nutritious? Didn’t you used to be vegan?

I’ve always had terrible health problems: stomach issues, migraines and allergies were the worst ones. I assumed it was because of my picky eating habits. Whenever I felt sick my mother would tell me it was because I didn’t eat enough vegetables. Then when I got to college I was diagnosed with gastroesophageal reflux disease and irritable bowel syndrome.

I read John Robbins’ Diet for a New America, which talked about how many common health ailments were related to diet, particularly animal products. I lived in a dormitory that had a vegetarian cafeteria and started eating there. A few things got better, but I still was on many medications. At one point I think I was on 13 different ones!

I was involved in several environmental groups and met many vegans that I admired. They convinced me that veganism was more logical than vegetarianism, since milk and eggs involve plenty of dead animals, so I cut those out too.

But I still didn’t feel great. When I moved into a dorm without a cafeteria I started experimenting with my diet. I did a pretty lengthy elimination diet and realized gluten was the probable cause of my GERD, but that other grains seemed to irritate my digestive system as well.

Did you try cutting out grains?

I did grain-free veganism for several months, but I struggled with chronic hunger. I would lapse by eating cheese at some public function and then feel gross and guilty. I ate at the local vegan restaurant, The Red Herring, as often as possible. But whenever I ate there I got sick.

Then I got really sick. It took my doctors some time to figure out what I had because they weren’t sure if my other illnesses had gotten worse or if I had a new illness. It turns out I had salmonella and that it had taken up residence. Most young people are able to clear salmonella within a few days, but it had tormented me for over a month. I had to go on some heavy duty antibiotics.

I fell into raw veganism because my digestive system was trashed and I thought maybe it would be the cure. So many people on raw vegan boards have stories about how it’s such a wonderful diet and because of it they are no longer sick. I believed them. I definitely felt much better… at first.

This is the common lament of raw veganism. It eliminates most problematic foods, but where is the nutrition? At this point I had been sick enough that I just wanted to get better and after reading Art De Vany’s writings on evolutionary diet and fitness, I decided to follow his recommendations.

[...]

What was your major?

I studied agricultural economics at the University of Illinois and then forest ecology at the Swedish University of Agriculture. I kept waffling between majors and so I took a diverse selection of courses — food/agricultural law, nutrition science, econometrics, environmental economics, entomology, development economics, toxicology, crop science and anthropology.

I plan on eventually doing a PhD in forestry or natural resource economics and I would also like to have my own farm.Fantastic article with a very smart lady! Melissa's blog Hunt, Gather, Love is excellent, and in this article she talks about her journey to paleo from veganism, and displays a deep knowledge of nutrition and dietary issues. I did the vegetarian thing for a few years after reading John Robbins’ Diet for a New America as well, and gained a ton of weight, weight which I struggled to lose. I went off vegetarianism after reading the book The Paleolithic Prescription, which was fascinating, and disabused me of my vegetarian philosophy.

In the U.S., public awareness of gluten free diets has reached widespread recognition, but largely in name only. For those suffering with celiac disease or acute wheat allergies, it’s critical. For those with known reactions to gluten, it’s of serious importance. For those who don’t really know what it’s about, but see it on packaging, it seems to evoke a similar response as being forced to “Press 1 for English”. Journalists tend to frame the gluten free approach as legit for celiac treatment, but ultimately a fad diet controlling minions of mindless Gwyneth Paltrow lovers (AP Article). The paleo diet community views it as more of a religion (that’s tongue-in-cheek hyperbole, people!). Before we continue, here are my biases: I experience repeatable, specific, and boring symptoms from gluten intake, but I do not have celiac disease or a “gluten allergy”. Evolutionary biology is a scientific fact and I believe the paleo diet provides ultimate explanations for why we should’t eat grains. So what are the proximate explanations for going gluten free? Is it fad or fo’ real?A quick and dirty primer

Celiac (or coeliac) disease is an autoimmune disorder in which the small intestine is damaged by components of gluten, a protein found in wheat and other grains. The effects of celiac diseas are numerous, serious, and varied. For a entertaining sobering look, check out Tim Ferriss’ How to Keep Feces Out of Your Bloodstream. Strictly speaking, a “wheat allergy” can be similar to something like a peanut allergy. Folks in this group experience rapid onset symptoms that are serious, including the potential of anaphylactic shock. It’s mainly for these folks that food is required to expose the presence of wheat content on packaging.

From there, we transition into the murky terms of gluten intolerance and/or sensitivity. These two classifications are where the non-celiac, non-allergy folks may reside. Whether we should take them seriously is what the references below try to answer. There’s plenty of research and anecdotal evidence within the paleo and related nutrition/health worlds. However, since they’re in it for the money, some people tend to pass what they say off as mere profiteering. And perhaps that’s fair, but perhaps both are justified.

Below are a series of links (and abstracts when available) to recent medical literature on gluten research. Basically, I just did a search on PubMed for articles with “gluten” in the title, but without “celiac” or “coeliac” in the title. Doing this search brought up 1340+ results, so I narrowed it down. I’ve tried to filter out the articles discussing the use of gluten free diets in the treatment of autism. I’ve also endeavored to filter out everything relating to animal studies. That said, some of the animal studies are quite convincing… But I get it… Humans aren’t chimpanzees or mice. Also, I only went back to 2008 (this was written in September, 2010).

[...]

Current Barometer

My assessment of the current barometer for medical research on the effect of gluten on humans is roughly this: In the general population (those not having celiac disease or wheat allergies), gluten either causes, or is strongly correlated to a range of autoimmune and neurological disorders. Further, gluten intolerance can present with any one, or group, of symptoms or disorders with varying degrees of severity. Lastly, it is generally agreed that celiac disease and non-celiac gluten intolerance are underreported and under-diagnosed, though the numbers remain speculative.

For me, on a practical level, the correlations between autoimmune and neurological problems in the scientific literature, my personal experiences with gluten, anecdotal reports from others, and the logical framework of evolutionary biology/paleo diet is convincing enough for me to abstain from gluten.

Andrew brings together a ton of great links to research studies showing the negative effects of gluten in this post on his blog, evolvify.com. I see many of these studies show the gluten link to schizophrenia, as seen in my last blog post below. Learning about celiac was a real revalation to me that started me on my own low carb journey. How can carbs be so essential to human health if a segment of the population is allergic to them? That's not how evolution works at all.

Dietary Sugar and Mental Illness: A Surprising LinkSugar and Mental Illness: A Surprising LinkPublished on July 23, 2009

Noted British psychiatric researcher Malcolm Peet has conducted a provocative cross-cultural analysis of the relationship between diet and mental illness. His primary finding may surprise you: a strong link between high sugar consumption and the risk of both depression and schizophrenia.

In fact, there are two potential mechanisms through which refined sugar intake could exert a toxic effect on mental health.

First, sugar actually suppresses activity of a key growth hormone in the brain called BDNF. This hormone promotes the health and maintenance of neurons in the brain, and it plays a vital role in memory function by triggering the growth of new connections between neurons. BDNF levels are critically low in both depression and schizophrenia, which explains why both syndromes often lead to shrinkage of key brain regions over time (yes, chronic depression actually leads to brain damage). There's also evidence from animal models that low BDNF can trigger depression.

Second, sugar consumption triggers a cascade of chemical reactions in the body that promote chronic inflammation. Now, under certain circumstances (like when your body needs to heal a bug bite), a little inflammation can be a good thing, since it can increase immune activity and blood flow to a wound. But in the long term, inflammation is a big problem. It disrupts the normal functioning of the immune system, and wreaks havoc on the brain.

Inflammation is associated with an increased risk of heart disease, diabetes, arthritis, and even some forms of cancer . . . it's also linked to a greater risk of depression and schizophrenia. And again, eating refined sugar triggers inflammation. So does eating heavily processed molecular cousins like 'high fructose corn syrup'.

Not surprising to me, ha ha! I've seen a good amount of evidence for this. Something as simple as sugar can have so many different effects in different people. It may be hard for people to believe that my obesity, Fred's depression, Mary's arthritis, and Joe's schizophrenia can all be traced to refined carbs, but the evidence is there. I read some interesting stuff a while back about "insulin shock" therapy. They gave people hyperdoses of insulin, putting them into a diabetic coma. Then later they would wake them up with a glucose injection. Sometimes it worked. One of the most famous people treated was physicist John Nash, portrayed by Russell Crowe in the movie A Beautiful Mind. Seems to me as if there's a connection between the insulin/sugar process and schizophrenia for some people. There's also evidence that cannabis use in susceptible users may encourage the development of schizophrenia. I'm not sure how solid that link is, and if it's based on simple correlation observed in epidemiological studies, which would not necessarily imply causation. But if there is a link, I wonder about the fact that some report that using cannibis can affect blood sugar, I believe by lowering it acutely, leading to the munchies. Speculation, but again, I like looking for links.

Starvation had long been one approach to treating epilepsy. Deny the patient food for, say, a week and often their seizures went away. But there were obvious limits on how long starvation could be used as a treatment. In the 1920s, researchers at the Mayo Clinic, looking for a way to treat diabetics, figured out that it was not fasting per se that helped control seizures. Rather, they found that it was what the body did during an extended fast that helped control them. Deprived of food, the human body starts burning body fat as fuel, and it was that process of ketosis that somehow had the antiepileptic effect. Trick the body into thinking it was starving by taking away its primary fuel of carbohydrates and forcing it to subsist on an all-fat diet, and you could create that antiepileptic effect as long as necessary.

The diet was quickly adopted and widely used through the 1930s. And then, almost as fast as it had appeared, the keto diet disappeared. When Dilantin was first used as an antiepileptic drug in 1938, its success steered medical minds toward pharmaceutical solutions. A generation later, the diet had been all but forgotten. There was no scientific evidence that it worked, after all. More important, it was incredibly difficult to administer. Even in the 1990s, Millicent Kelly, Charlie Abrahams’s dietitian at Johns Hopkins, was planning menus with a calculator and a legal pad.

By 2000, more people were asking about keto, but most pediatric neurologists still would not prescribe it. That bias seemed ridiculous to J. Helen Cross, the principal investigator of the 2008 randomized keto trial at University College London. “I’d been dealing with complex epilepsy cases for 10 years, and it was quite clear to me that certain children did respond to the ketogenic diet,” Cross says. “But we in our institution — and I know we weren’t alone — were coming up against barriers to get the resources to do it. They’d say there’s no evidence it works. It’s a quack diet. There is no controlled data. So I wanted to prove that it did work once and for all, and do it in a way so that people couldn’t argue with it.”

It took five years to enroll and track enough patients to make the study credible and another two years to analyze the data and undergo the rigorous academic peer-review process. But since the study was published in 2008, it has answered doubts about keto’s clinical effectiveness.

Keto has now attracted attention from all corners of the neurological community. Two scientists at the National Institutes of Health are planning a study of its effectiveness in Parkinson’s patients. Papers published in the past two years suggest that keto may slow the growth of a brain tumor in mice. A biotechnology company named Accera is marketing a high-fat powder to Alzheimer’s patients that is supposed to reproduce the effects of ketosis, without the dietary restrictions of keto.

Still, there is one giant unanswered question: Why does keto work? Jong Rho, the head of pediatric neurology at the University of Calgary and the Alberta Children’s Hospital, theorizes that ketone bodies — the compounds made by the liver when the body burns fat for energy — protect brain cells from being damaged. Rho, who just received a $2 million, five-year grant from the National Institutes of Health to continue to investigate this theory, says experiments with epileptic mice suggest that extended time on the diet makes them more seizure-resistant.

Rho’s theory, however, only raises more questions. How would ketone bodies protect brain cells? Scientists don’t have a clue about how our cells react during ketosis. They don’t even know how much ketone bodies themselves matter. Until scientists understand the basic biological mechanisms, they can’t begin to embark on the long and costly process of drug development.

The success of the pediatric diet seems to have made it easier for keto scientists to get money for this basic research. “Before Helen’s study, we all had a clear sense that keto worked,” says Carl Stafstrom, the head of pediatric neurology at the University of Wisconsin, “but we couldn’t say in a grant proposal that the diet has been proven to be effective. Now we can.” There are recently financed studies, for example, exploring why the body resists ketosis and exploring compounds that might trigger the antiepileptic mechanism.

[...]

There has been so much buzz around keto that neurologists and scientists have begun wondering what else it can do. Could it be used to treat seizures in adults? What about Parkinson’s, Alzheimer’s, A.L.S. and certain cancers? Tumors typically need glucose to grow. There is very little of this simple sugar in a keto diet, and there have been interesting results with mice that suggest the diet might slow tumor growth. These scientific explorations are in their early stages and may not amount to much. Nonetheless, researchers are taking them seriously.

Fantastic article on the ketogenic diet for the treatment of epilepsy.

CHICAGO (Reuters) – A device that destroys nerves leading to the kidney safely lowered blood pressure in people with treatment-resistant hypertension, potentially offering a new option for millions of people who struggle to keep their disease in check, researchers said on Wednesday.

The device, made by privately held Ardian Inc of Mountain View, California, lowered the top blood pressure reading by an average of 32 points after six months, compared with no change in patients who took the best available medicines.

"There are a lot of questions, but it is very exciting," said Dr. Suzanne Oparil of the University of Alabama at Birmingham, who reviewed the findings presented at the American Heart Association meeting in Chicago.

The one-time treatment works by silencing nerves leading into and out of the kidney, which play a central role in the sympathetic nervous system, the body's "fight or flight" response that can increase heart rate and blood pressure.

Procedures that surgically disrupt these nerves had been shown to lower high blood pressure decades ago, but were abandoned with the advent of drugs that target the renin-angiotensin system, which regulates blood pressure and fluid retention.

"Those drugs are good but not perfect," said Dr Murray Esler of the Baker IDI Heart and Diabetes Institute in Melbourne, Australia, whose findings were released online by the Lancet.

"We can see that because of their failure in the patients on this trial. They are all on drugs of this type."

BLOOD PRESSURE READING FELL BY 32 POINTS

High blood pressure, or too much force exerted by blood as it moves against vessel walls, is the leading risk factor for premature death worldwide.

Nearly half of Europeans have hypertension, and in the United States, about 75 million Americans do -- and only two-thirds of those people are treated. Among those who are, half do not get their blood pressure under control.

Normal blood pressure is considered to be 120 over 80 or lower. A top reading of over 140 is considered high blood pressure.

[...]

After six months, blood pressure among those who got the treatment fell by 32 points on the top reading and 12 points on the bottom reading, pushing some into the near-normal range. There was no change in the control group.

"It was a big effect," Esler said. "The main pressure in the group after denervation was 145, and in 39 percent of them, it was 140 systolic."

"It's a much bigger effect than you would anticipate in a drug trial, particularly in these people, who are resistant to drugs anyway," Esler said. Very, very interesting. Especially the part about the kidneys and the sympathetic nervous system being a controlling element of hypertension. I was able to dig up other info on the kidney-hypertension link, and it's pretty solid. Low carb and/or fasting is a more natural treatment option. The low carb route also helps the other parts of metabolic syndrome (low HDL, high Triglcyerides, abdominal obesity, high blood sugar, and hypertension), whereas this treatment only affects one. I'm curious why it doesn't seem to affect the other factors, and also wonder if it has any effect on mortality. In other words, does a treat a symptom of metabolic disorder, but not improve the underlying problem?

A statistical comparison of results showed that few if any heart attacks or strokes would have been prevented within five years had anyone taken the medication, unless there was already some calcium buildup in their blood vessels. In people with moderate calcium buildup, one heart attack would have been averted in every 94 people treated, and one stroke in every 54.

For people with higher coronary calcium scores, the numbers of patients one needed to treat to prevent a heart attack or stroke were 24 and 19, respectively, which Blaha says were superior numbers to those in the JUPITER study or any prior statin trial.

According to study co-investigator and cardiologist Roger Blumenthal, M.D., a professor and director of the Ciccarone Preventive Cardiology Center at Johns Hopkins, "statin therapy should not be approached like diet and exercise as a broadly based solution for preventing coronary heart disease.

Statins are worth billions of dollars each year, and big pharma pushes doctors to push all of us to take them. Push back.

Many Americans aim to eat low-fat foods but there is strong evidence that replacing fat with carbohydrates could be harmful to health, according to nutrition experts at the ADA conference in Boston last week.

Recommendations to reduce saturated fat intake are largely based on the notion that high levels increase risk of cardiovascular disease, but unless saturated fat is replaced with other fats, many studies have suggested that fat reduction could increase risk of heart disease.

During a symposium called “The Great Fat Debate: Is There Validity In the Age-Old Dietary Guidance?” at the American Dietetic Association’s (ADA) Food and Nutrition Conference and Expo, four leading experts presented evidence suggesting that low fat diets may be less healthy than those containing at least a moderate amount of fat. In particular, all four agreed that replacing saturated fat with carbohydrates – as has been widely recommended in the United States – is likely to raise the risk of cardiovascular disease.

The low fat message

Director of the cardiovascular health laboratory at Tufts University Dr. Alice Lichtenstein said dietary advice to adhere to a low fat diet is based on an oversimplification of recommendations.

[...]

“If anything, the literature shows a slight advantage of the high fat diet,” he said. “The focus on fat in dietary guidelines has been a massive distraction…We should remove total fat from nutrition facts panels on the back of packs.”

He added that while the pervasive dietary guidance given to consumers has been to eat fats sparingly, to load up on starch and eat non-fat products, “the food industry quickly realized sugar was cheaper than fat and laughed all the way to the bank.”

“It was really the type of fat that was important,” he said. “If you replaced saturated fat with polyunsaturated fat there was a reduction of risk.”

American eating behavior

[...]

Assistant professor of medicine at Harvard Medical School Dr. Mozaffarian agreed with the other speakers about a lack of evidence linking total fat consumption and cardiovascular disease risk.

High levels of low density lipoprotein (LDL cholesterol) and high triglyceride levels have both been linked to increased risk of cardiovascular disease, but Mozaffarian said there has often been overreliance on single biomarkers in drawing conclusions about fats’ impact on heart health, “even one as hallowed as LDL cholesterol”.

“Overall dietary quality is very important for cardiovascular risk,” he said. “Saturated fats may raise LDL cholesterol but increasing levels of all fats lowers triglycerides…You can’t look at data across countries and draw conclusions. Nor can you look at animal studies or a single biomarker and draw conclusions from that.”

Concluding the discussion, Dr. Lichtenstein warned against focusing on single nutrients for disease risk reduction.

She said: “We need to stop focusing on individual dietary components because when one goes down, another goes up.”

Wow, this is unbelievable. The American Dietetic Association is the bastion of Low Fat dogma. The fact that they are allowing dissenting voices is laudable and surprising. As positive evidence for low carb diets continues to mount, dietary advice is beginning to change as well. There is still much we don't know, but the biggest thing is to drop the dogma, do more research, and keep an open mind. Very good news here.

A frequently cited concern of very-low-carbohydrate diets is the potential for increased risk of renal disease associated with a higher protein intake. However, to date, no well-controlled randomized studies have evaluated the long-term effects of very-low-carbohydrate diets on renal function. To study this issue, renal function was assessed in 68 men and women with abdominal obesity (age 51.5±7.7 years, body mass index [calculated as kg/m2] 33.6±4.0) without preexisting renal dysfunction who were randomized to consume either an energy-restricted (∼1,433 to 1,672 kcal/day), planned isocaloric very-low-carbohydrate (4% total energy as carbohydrate [14 g], 35% protein [124 g], 61% fat [99 g]), or high-carbohydrate diet (46% total energy as carbohydrate [162 g], 24% protein [85 g], 30% fat [49 g]) for 1 year. Body weight, serum creatinine, estimated glomerular filtration rate and urinary albumin excretion were assessed before and after 1 year (April 2006-July 2007). Repeated measures analysis of variance was conducted. Weight loss was similar in both groups (very-low-carbohydrate: −14.5±9.7 kg, high-carbohydrate: −11.6±7.3 kg; P=0.16). By 1 year, there were no changes in either group in serum creatinine levels (very-low-carbohydrate: 72.4±15.1 to 71.3±13.8 μmol/L, high-carbohydrate: 78.0±16.0 to 77.2±13.2 μmol/L; P=0.93 time × diet effect) or estimated glomerular filtration rate (very-low-carbohydrate: 90.0±17.0 to 91.2±17.8 mL/min/1.73 m2, high-carbohydrate: 83.8±13.8 to 83.6±11.8 mL/min/1.73 m2; P=0.53 time×diet effect). All but one participant was classified as having normoalbuminuria at baseline, and for these participants, urinary albumin excretion values remained in the normoalbuminuria range at 1 year. One participant in high-carbohydrate had microalbuminuria (41.8 μg/min) at baseline, which decreased to a value of 3.1 μg/min (classified as normoalbuminuria) at 1 year.

This study provides preliminary evidence that long-term weight loss with a very-low-carbohydrate diet does not adversely affect renal function compared with a high-carbohydrate diet in obese individuals with normal renal function.

The myth that low carb hurts your kidneys refuses to die. Here's one more stake in the heart for it.

Saturday, November 13, 2010

Our findings clearly demonstrate that intense sweetness can surpass cocaine reward, even in drug-sensitized and -addicted individuals. We speculate that the addictive potential of intense sweetness results from an inborn hypersensitivity to sweet tastants. In most mammals, including rats and humans, sweet receptors evolved in ancestral environments poor in sugars and are thus not adapted to high concentrations of sweet tastants. The supranormal stimulation of these receptors by sugar-rich diets, such as those now widely available in modern societies, would generate a supranormal reward signal in the brain, with the potential to override self-control mechanisms and thus to lead to addiction.

I'm sure many people would nod their heads in agreement with the assertion that sweet treats are addictive. What was once a rare treat for our paleo ancestors is now everywhere, and hard to say no to. There's some evidence that upping magnesium intake may help people deal with sugar cravings. I have some magnesium articles on my blog here. Stick around and take a look!

Newswise — Contrary to earlier research, a new, long-term study suggests that cholesterol level in mid-life may not be linked to later development of Alzheimer’s disease, according to a study published in the November 10, 2010, online issue of Neurology®, the medical journal of the American Academy of Neurology. However, the results suggest that large decreases in cholesterol levels in old age could be a better predictor of developing the memory-robbing disease.

“While some studies suggest that cholesterol is a risk factor for dementia, others have not replicated this finding, so the possible association has been under debate,” said study author Michelle M. Mielke, PhD, with Johns Hopkins University School of Medicine in Baltimore.

At first, humans were not terribly good hunters. They started out as scavengers who trailed behind predators such as lions and ate the leftovers remaining on abandoned carcasses. The pickings were slim; ravenous lions don't leave much behind, except for bones. But with their handy tools (stone anvils and hammers), our early ancestors could crack the skulls and bones and still find something to eat -- brains and fatty marrow.

Marrow fat was the main concentrated energy source that enabled the early human gut to shrink, while the scavenged brains contained a specific type of omega 3 fat called "docosahexaenoic acid" (DHA), which allowed the brain to expand. Docosahexaenoic acid is the building block of our brain tissue.

Without a dietary source of DHA, the huge expansion of our brain capacity could never have happened. Without meat, marrow, and brains, our human ancestors never would have been able to walk out of tropical Africa and colonize the colder areas of the world. If these people had depended on finding plant foods in cold Europe, they would have starved. In a landmark series of studies, my colleague Mike Richards, at Oxford University, studied the bones of Paleolithic people who lived in England some 12,000 years ago. Their diet, Richards confirmed, was almost identical to that of top-level carnivores, such as wolves and bears.

[...]

The archaeological record clearly shows that whenever and wherever ancient humans sowed seeds (and replaced the old animal-dominated diets), part of the harvest included health problems. One physical ramification of' the new diet was immediately obvious: Early farmers were markedly shorter than their ancestors. In Turkey and Greece, for example, preagricultural men stood 5 feet 9 inches tall and women 5 feet 5 inches. By 3000 the average man had shrunk to 5 feet 3 inches and the average woman to 5 feet. But getting shorter -- not in itself a health problem -- was the least of the changes in these early farmers. Studies of their bones and teeth have revealed that these people were basically a mess: They had more infectious diseases than their ancestors, more childhood mortality, and shorter life spans in general.

Teeth

They also had more osteoporosis, rickets, and other bone mineral disorders, thanks to the cereal-based diets. For the first time, humans were plagued with vitamin and mineral-deficiency diseases -- scurvy, beriberi, pellagra, vitamin A and zinc deficiencies, and iron-deficiency anemia. Instead of the well-formed, strong teeth their ancestors had, there were now cavities. Their jaws, which were formerly square and roomy, were suddenly too small for their teeth, which overlapped each other.

Friday, November 12, 2010

A long time ago, by the shores of a lake in East Africa, a group of hungry foragers tucked into a primeval steak dinner. They carved the meat of cow- and goat-sized animals with sharp stone tools and smashed the bones to get at the rich marrow inside. The scene is remarkable mainly because it happened 3.4 million years ago, pushing back by 800,000 years the earliest known example of hominids using stone tools and eating meat.

The foragers in question were likely members of the primitive genus Australopithecus, specifically A. afarensis, the species to which the celebrated Lucy fossil belongs. Scientists had long believed that the australopithecines, whose teeth and jaws were adapted for eating fruit, seeds and other plant foods, were primarily vegetarian. But the new finds—cut-marked animal bones recovered from a site called Dikika, just a few kilometers from the Lucy site in Ethiopia’s Afar region—suggest that “we could now be looking at an extended period of time when [hominids] were including meat in their diet and experimenting with the use of stone tools,” observes lead study author Shannon P. Mc­Pher­ron of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. A report describing the bones appeared in the August 12 issue of Nature.

Wednesday, November 10, 2010

Children with hypertension more likely to have learning disabilities, ADHD10. November 2010 01:06

Children who have hypertension are much more likely to have learning disabilities than children with normal blood pressure, according to a new University of Rochester Medical Center (URMC) study published this week in the journal, Pediatrics. In fact, when variables such as socio-economic levels are evened out, children with hypertension were four times more likely to have cognitive problems.

"This study also found that children with hypertension are more likely to have ADHD (attention deficit hyperactivity disorder)," said Heather R. Adams, Ph.D., an assistant professor of Neurology and Pediatrics at URMC, and an author of the study. "Although retrospective, this work adds to the growing evidence of an association between hypertension and cognitive function. With 4 percent of children now estimated to have hypertension, the need to understand this potential connection is incredibly important."

Researchers say there's a link between childhood ADHD and adult obesity, and the greater the number of ADHD symptoms a child has the more likely they may be to be overweight in adulthood. The study looked at symptoms of inattention, hyperactivity, and impulsivity along with body mass index for 15,197 teens who were studied between 1995 and 2009.

I saw a figure once that 70% of morbidly obese people have ADD. I really think there's a connection here. Scientists are beginning to learn that the brain itself can become insulin resistant. Perhaps that's why many people who do low carb or ketogenic diets to lose weight find themselves thinking more clearly, have more drive and a better mood.

Naloxone (IV) and naltrexone (oral) are drugs that block the action of morphine.

If you were an inner city heroine addict and got knifed during a drug deal, you'd be dragged into the local emergency room. You're high, irrational, and combative. The ER staff restrain you, inject you with naloxone and you are instantly not high. Or, if you overdosed on morphine and stopped breathing, an injection of naloxone would reverse the effect immediately, making you sit bolt upright and wondering what the heck was going on.

So what do morphine-blocking drugs have to do with weight loss?

An odd series of clinical studies conducted over the past 40 years has demonstrated that foods can have opiate-like properties. Opiate blockers, like naloxone, can thereby block appetite. One such study demonstrated 28% reduction in caloric intake after naloxone administration. But opiate blocking drugs don't block desire for all foods, just some.

What food is known to be broken down into opiate-like polypeptides?

Wheat. On digestion in the gastrointestinal tract, wheat gluten is broken down into a collection of polypeptides that are released into the bloodstream. These gluten-derived polypeptides are able to cross the blood-brain barrier and enter the brain. Their binding to brain cells can be blocked by naloxone or naltrexone administration. These polypeptides have been named exorphins, since they exert morphine-like activity on the brain. While you may not be "high," many people experience a subtle reward, a low-grade pleasure or euphoria.

For the same reasons, 30% of people who stop consuming wheat experience withdrawal, i.e., sadness, mental fog, and fatigue.

Wouldn't you know that the pharmaceutical industry would eventually catch on? Drug company startup, Orexigen, will be making FDA application for its drug, Contrave, a combination of naltrexone and the antidepressant, buproprion. It is billed as a blocker of the "mesolimbic reward system" that enhances weight loss.

Step back a moment and think about this: We are urged by the USDA and other "official" sources of nutritional advice to eat more "healthy whole grains." Such advice creates a nation of obese Americans, many the unwitting victims of the new generation of exorphin-generating, high-yield dwarf mutant wheat. A desperate, obese public now turns to the drug industry to provide drugs that can turn off the addictive behavior of the USDA-endorsed food.

There is no question that wheat has addictive properties. You will soon be able to take a drug to block its effects. That way, the food industry profits, the drug industry profits, and you pay for it all.

Tuesday, November 09, 2010

Overweight children reported more frequent intake of healthy foods such as fruit, vegetables, fish, brown bread and potatoes as well as low-energy cheese and yoghurt compared with normal weight children. This comes from a recent study from researchers at Telemark University College and the Norwegian Institute of Public Health.

The study showed that:

* Overweight children drank juice and artificially sweetened soft drinks more often, while the normal weight children drank carbonated drinks and ate unhealthy foods and processed foods such as burgers, sausages, biscuits, processed pizza and sweets. * The results suggest that both parents and children have increased awareness of food choices when children are overweight. * The study also showed that overweight children were less physically active and were more likely to have obese parents than normal weight children.

"It is positive that parents and children emphasise healthy food choices. However, it is important to note that the amount of healthy foods must be adapted to a child's activity level to limit further weight gain," said researcher Anne Lise Brantsæter at the NIPH.

Reference:IM Oellingrath, MV Svendsen, AL Brantsæter. Eating patterns and overweight in 9- to 10-year-old children in Telemark County, Norway: a cross-sectional study. European Journal of Clinical Nutrition. 18. August 2010.

Lol, maybe the juice, fruit, bread, potatoes and low fat cheese made the kids fat. Cause you know if the study said the kids ate more meat it would be seen as "proof" meat causes obesity. Just sayin'

Around 25,000 people in the UK have narcolepsy, a condition characterised by sudden and uncontrollable episodes of deep sleep, often at times of stress or even sexual arousal. There's no known cure, but in terms of medical advances, 2010 has been lively.

As well as the reported alleged links to the swine flu vaccine in August – still unproven – Swiss researchers claimed in February to have identified the overproduction of an antibody, Trib2, in the immune systems of narcoleptics. Scientists at Geneva and Lausanne universities believe Trib2 is responsible for destroying hypocretin-secreting neurons in the brain. Hypocretin is a hormone that regulates sleep, so low levels interfere with non-REM (rapid-eye-movement) sleep and makes staying awake for long periods a struggle.

Excitingly, the tests suggested this damage could potentially be stabilised with intravenous immunoglobulin, a laboratory-made antibody. If patients could be diagnosed and treated within a year of symptoms presenting – when the antibodies are at their most destructive levels – the illness's impact could be greatly reduced. "There is a chance to save some of the hypocretin cells at early onset," says Professor Adrian Williams, who runs the sleep disorders centre at St Thomas's Hospital, London, and this year became the UK's first Chair in Sleep Medicine. "Unfortunately, narcolepsy is still under-recognised, and it is typically a few years between onset of symptoms – usually in the teens – and diagnosis."

Other studies indicate environmental factors that could "switch on" the gene for narcolepsy, which exists in a third of the population. In June, a Journal of Sleep Research paper reported a five-fold increase of the condition among genetically predisposed individuals who had suffered bacterial throat infections in childhood, while US studies suggested that exposure to heavy metals and gardening chemicals, as well as passive smoking, could be a trigger.

Perhaps the most significant development of recent years has been a medicine, Xyrem, whose active ingredient, sodium oxybate, is a derivative of the illicit substance GHB. Licensed here since 2006, it works by mimicking the activity of hypocretin.

Fish and other seafood are rich sources of the omega-3 fatty acids known as DHA and EPA, which have been found to provide protection from chronic diseases, such as type 2 diabetes, said LSU AgCenter nutritionist Beth Reames.

(Media-Newswire.com) - Fish and other seafood are rich sources of the omega-3 fatty acids known as DHA and EPA, which have been found to provide protection from chronic diseases, such as type 2 diabetes, said LSU AgCenter nutritionist Beth Reames.

In recent studies with animals, U.S. Department of Agriculture researchers have found that DHA provided protection against insulin resistance and nonalcoholic fatty liver disease, and EPA offered partial protection against fatty liver disease.

Insulin resistance is a condition in which the body isn’t able to efficiently use its own insulin to remove glucose from the bloodstream, Reames said. If left untreated, insulin resistance can lead to harmful buildup of glucose in the bloodstream and diabetes.

Nonalcoholic fatty liver disease results from accumulation of excess fat in the liver and may be caused by diabetes and obesity, Reames said. Afflicted liver tissue may harden and scar, sometimes resulting in cirrhosis of the liver or liver cancer.

“Human studies of the effects of DHA and EPA on insulin resistance have been inconclusive,” Reames said. “The researchers recommend new investigations, with larger numbers of volunteers, to more clearly define the relation of DHA and EPA to insulin resistance in humans.”

To get DHA and EPA in your diet, nutritionists recommend eating fatty or oily fish, including mackerel, sardines, anchovies, herring, albacore tuna and salmon, as well as oysters, shrimp, crawfish and fish oil supplements. In addition, omega-3 fatty acids are available from plant sources including soybean oil, canola oil, flaxseed and walnuts.

Omega-3 fatty acids help relax the arteries and improve blood circulation to the heart, inhibit blood clotting and improve heartbeat. They lower triglycerides and lower blood pressure. These factors make heart attacks less likely. They also keep the arteries open by discouraging the buildup of plaque in blood vessels.

Along with omega-3 fatty acids, fish and seafood offer additional health benefits. They are nutrient-dense and packed with protein.

Saturday, November 06, 2010

AbstractThis paper presents the published and unpublished stable carbon and nitrogen isotope values for 36 European Upper Paleolithic humans from 20 sites. The isotope data were measured to determine the sources of dietary protein in Upper Paleolithic diets; the evidence indicates that animal, not plant, protein was the dominant protein source for all of the humans measured. Interestingly, the isotope evidence shows that aquatic (marine and freshwater) foods are important in the diets of a number of individuals throughout this period.

Received 21 January 2010; accepted 18 September 2010. published online 01 November 2010.Corrected ProofAbstract

The purpose of this study was to determine if a high-fat diet would result in a higher lipolytic rate in subcutaneous adipose tissue than a lower-fat diet in sedentary nonlean men. Six participants (healthy males; 18-40 years old; body mass index, 25-37 kg/m2) underwent 2 weeks on a high-fat or well-balanced diet of similar energy content (approximately 6695 kJ) in randomized order with a 10-day washout period between diets. Subcutaneous abdominal adipose tissue lipolysis was determined over the course of a day using microdialysis after both 2-week diet sessions. Average interstitial glycerol concentrations (index of lipolysis) as determined using microdialysis were higher after the high-fat diet (210.8 ± 27.9 μmol/L) than after a well-balanced diet (175.6 ± 23.3 μmol/L; P = .026). There was no difference in adipose tissue microvascular blood flow as determined using the microdialysis ethanol technique. These results demonstrate that healthy nonlean men who diet on the high-fat plan have a higher lipolytic rate in subcutaneous abdominal adipose tissue than when they diet on a well-balanced diet plan. This higher rate of lipolysis may result in a higher rate of fat mass loss on the high-fat diet; however, it remains to be determined if this higher lipolytic rate in men on the high-fat diet results in a more rapid net loss of triglyceride from the abdominal adipose depots, or if the higher lipolytic rate is counteracted by an increased rate of lipid storage.

Thursday, November 04, 2010

Along with the saturated fat and cholesterol scares of the past several decades has come the notion that vegetarianism is a healthier dietary option for people. It seems as if every health expert and government health agency is urging people to eat fewer animal products and consume more vegetables, grains, fruits and legumes. Along with these exhortations have come assertions and studies supposedly proving that vegetarianism is healthier for people and that meat consumption causes sickness and death. Several medical authorities, however, have questioned these data, but their objections have been largely ignored.

As we shall see, many of the vegetarian claims cannot be substantiated and some are simply false and dangerous. There are benefits to vegetarian diets for certain health conditions, and some people function better on less fat and protein, but, as a practitioner who has dealt with several former vegans (total vegetarians), I know full well the dangerous effects of a diet devoid of healthful animal products.

It is my hope that all readers will more carefully evaluate their position on vegetarianism after reading this article. It is important to note that there are different types of vegetarianism, including lacto-vegetarian diets (dairy products included) and lacto-ovo-vegetarian diets (dairy products and eggs included). The nutritional caveats that follow are primarily directed at veganism, or a diet totally lacking in animal products.

Received 25 July 2008; Revised 20 November 2008; Accepted 30 December 2008; Published online 11 February 2009.Top of pageAbstractBackground:

The contemporary American diet figures centrally in the pathogenesis of numerous chronic diseases—‘diseases of civilization’. We investigated in humans whether a diet similar to that consumed by our preagricultural hunter-gatherer ancestors (that is, a paleolithic type diet) confers health benefits.Methods:

We performed an outpatient, metabolically controlled study, in nine nonobese sedentary healthy volunteers, ensuring no weight loss by daily weight. We compared the findings when the participants consumed their usual diet with those when they consumed a paleolithic type diet. The participants consumed their usual diet for 3 days, three ramp-up diets of increasing potassium and fiber for 7 days, then a paleolithic type diet comprising lean meat, fruits, vegetables and nuts, and excluding nonpaleolithic type foods, such as cereal grains, dairy or legumes, for 10 days. Outcomes included arterial blood pressure (BP); 24-h urine sodium and potassium excretion; plasma glucose and insulin areas under the curve (AUC) during a 2 h oral glucose tolerance test (OGTT); insulin sensitivity; plasma lipid concentrations; and brachial artery reactivity in response to ischemia.Results:

Compared with the baseline (usual) diet, we observed (a) significant reductions in BP associated with improved arterial distensibility (−3.1±2.9, P=0.01 and +0.19±0.23, P=0.05);(b) significant reduction in plasma insulin vs time AUC, during the OGTT (P=0.006); and (c) large significant reductions in total cholesterol, low-density lipoproteins (LDL) and triglycerides (−0.8±0.6 (P=0.007), −0.7±0.5 (P=0.003) and −0.3±0.3 (P=0.01) mmol/l respectively). In all these measured variables, either eight or all nine participants had identical directional responses when switched to paleolithic type diet, that is, near consistently improved status of circulatory, carbohydrate and lipid metabolism/physiology.Conclusions:

Concerns that were raised with the first dietary recommendations 30 y ago have yet to be adequately addressed. The initial Dietary Goals for Americans (1977) proposed increases in carbohydrate intake and decreases in fat, saturated fat, cholesterol, and salt consumption that are carried further in the 2010 Dietary Guidelines Advisory Committee (DGAC) Report. Important aspects of these recommendations remain unproven, yet a dietary shift in this direction has already taken place even as overweight/obesity and diabetes have increased. Although appealing to an evidence-based methodology, the DGAC Report demonstrates several critical weaknesses, including use of an incomplete body of relevant science; inaccurately representing, interpreting, or summarizing the literature; and drawing conclusions and/or making recommendations that do not reflect the limitations or controversies in the science. An objective assessment of evidence in the DGAC Report does not suggest a conclusive proscription against low-carbohydrate diets. The DGAC Report does not provide sufficient evidence to conclude that increases in whole grain and fiber and decreases in dietary saturated fat, salt, and animal protein will lead to positive health outcomes. Lack of supporting evidence limits the value of the proposed recommendations as guidance for consumers or as the basis for public health policy. It is time to reexamine how US dietary guidelines are created and ask whether the current process is still appropriate for our needs.

FANTASTIC take down of the latest dietary guidelines for americans, 2010 version. This is the report behind the food pyramid, mypyramid, and mypyramid.gov. Basically the whole food pyramid is based on sloppy science, and more importantly, misrepresenting the science that's out there. This report here just shreds the dietary guidelines put out by the federal government. Basically the evidence for fiber, fruits and vegetables, and low fat eating is just not there, despite decades of research designed to "prove" the lipid hypothesis. The feds keep trying to force a square peg into a round hole. Bottom line, avoid sugar, grains (especially processed), eat some fruits and veges, but don't get obsessive about it, and eat lots of quality meat. I would add preferably grassfed meat, and wild caught seafood. Real food, mostly meat, some plants, to paraphrase the author of the Omnivore's dilemma.

Researchers from of the Center for Obesity Research and Education at Temple University, Philadelphia have revealed that after a two-year comparison, a low-carb diet fares about as well as a low-fat diet with regards to weight loss, but low-carb improves cardiovascular risk factors more.

The study, published in the peer-reviewed medical journal Annals of Internal Medicine, explained that cardiovascular risk factors, such as blood pressure and lipid (cholesterol) levels responded better with the low-carb diet. Both diets produce identical weight loss when coupled with comprehensive behavior treatment

Put simply - it appears that both diets are equally good for losing weight, but the low-carb diet protects you from potential coronary heart diseases more effectively.

[...]

Among the participants in the two diet groups, the researchers found:

* Weight - no differences at any point during the study. About 7% loss of weight at two years in both groups. * Body composition - no differences at any point during the study * Bone mineral density - no differences at any point during the study * Good cholesterol levels - double the increase among the low-carb group compared to the low-fat group at two years. 23% and 11% respectively.

More and more good research coming out on low carb the last few years, all of it good. When Atkins was big, people said "where's the evidence that this way of eating works and is safe?", but studies had not been done, because researchers were busy trying fruitlessly to "prove" fat was bad. Now that the attention is focused on low carb, the consensus of the research seems to indicate same or greater weight loss, on low carb vs. low fat, but much better readings on blood pressure, HDL, cholesterol, triglycerides, etc. This study is one of many.

There may be a fundamental link between aspects of an individual's personality and their capacity to exercise or generate energy, recent research suggests.

Humans are not the only animals that choose to exercise and - as with people - individuals within the same species differ in their levels of activity, says Dr Peter Biro, a senior lecturer in the UNSW Evolution and Ecology Research Centre, in a review article in the journal Trends in Ecology and Evolution, with colleague Judy Stamps of the University of California, Davis. Dr Biro is an Australian Research Council Future Fellow.

Likewise, scientists now recognise that many animals have 'personality', in that they display consistent differences in behaviours. Dr Biro believes it is significant that those behaviours often relate to the rates at which they acquire and expend energy through feeding or activity.

"Some of us are couch potatoes while others are drawn to sport and exercise," notes Dr Biro. "We often associate the athletic 'jock' type or person with being aggressive and social, whereas the more sedentary 'nerd' often is seen as more socially awkward and submissive.

"These are generalisations, but most people would probably agree there is some truth to them. If so, why should individuals differ in their propensity for activity and in their personality, and why might they be related? "

The article reviews a wide range of recent research into these questions and concludes that there is now enough evidence to suggest a link between an individual's personality and the rate of its metabolism - the chemical process that converts food into the energy that fuels the body.

"Animals in captivity often engage in energetically demanding behaviour when they have unlimited food available," Dr Biro says. "Mice spend considerable time on running wheels, for example, and other animals often pace back and forth in zoo enclosures. Given they don't need to move about in search of food as they would in nature, we might ask why they are apparently 'exercising'.

"Recent research suggests that this behaviour might be related to an individual's capacity to generate energy - its 'metabolic capacity'. For example, mice in isolation that have high metabolism tend spend more time on running wheels, and run faster, than those with low metabolism.

"Male crickets with sex on their mind tend to call to attract mates more and have higher metabolism than those with slower metabolism."

Metabolism and aggression are also linked. It has now been documented, for example, in several species of fish and birds that individuals with high metabolism tend to be more aggressive and dominant over those with slow metabolism.

The amount of energy devoted to energetically demanding activities differs among individuals, Dr Biro says. These differences in energetic capacity - along with the tendency for metabolism to be consistent over long periods - might provide a very general explanation for personality in animals.

"It may just be that some individuals generate much more energy than others and when those individuals are captive with abundant food, they must outlet 'excess' energy that is normally expressed in nature in activities such as feeding and defence of food supplies.

"We are still some ways from a really solid understanding of the links between metabolism and personality in animals, but recent research suggests these ideas have merit and are worth studying further."

According to a new study being published in Annals of Internal Medicine, the flagship journal of the American College of Physicians, lack of sleep may hinder a dieter's ability to shed excess body fat.

Ten overweight but otherwise healthy adults on a moderate calorie-restricted diet were randomly assigned to sleep either 5.5 hours or 8.5 hours each night in a closed clinical research environment. After two weeks, researchers measured loss of fat and lean body mass. Compared to participants who slept 5.5 hours a night, the dieters that slept for 8.5 hours lost 56 percent more body fat. The dieters in the sleep restricted group had lost less fat and more lean body mass.

"These results highlight the importance of adequate sleep for maintenance of fat-free body mass when dieting to lose weight," said Plamen Penev, MD, PhD, Assistant Professor, Section of Endocrinology, at the University of Chicago and lead author of the study.

While measuring fat loss was the primary objective of the study, researchers also assessed other factors including levels of hormones that affect the appetite and weight. In addition, participants in both groups were asked to report how much hunger they experienced during the study.

"Among other hormonal effects, we found that sleep restriction caused an increase in ghrelin levels in the blood," said Dr. Penev. "Ghrelin is a hormone that has been shown to reduce energy expenditure, stimulate hunger and food intake, promote retention of fat, and increase glucose production in the body. This could explain why sleep-deprived participants also reported feeling hungrier during the study."

Olefsky and colleagues looked at cellular receptors known to respond to fatty acids. They eventually narrowed their focus to a G-protein receptor called GPR120, one of a family of signaling molecules involved in numerous cellular functions. The GPR120 receptor is found only on pro-inflammatory macrophages in mature fat cells. When the receptor is turned off, the macrophage produces inflammatory effects. But exposed to omega-3 fatty acids, specifically docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), the GPR120 receptor is activated and generates a strong anti-inflammatory effect.

Olefsky, a professor of medicine and associate dean of scientific affairs for the UC San Diego School of Medicine stated that, "It's just an incredibly potent effect… The omega-3 fatty acids switch on the receptor, killing the inflammatory response."

The scientists conducted their research using cell cultures and mice, some of the latter genetically modified to lack the GPR120 receptor. All of the mice were fed a high-fat diet with or without omega-3 fatty acid supplementation. The supplementation treatment inhibited inflammation and enhanced insulin sensitivity in ordinary obese mice, but had no effect in GPR120 knockout mice. A chemical agonist of omega-3 fatty acids produced similar results.

"This is nature at work," said Olefsky. "The receptor evolved to respond to a natural product -- omega-3 fatty acids -- so that the inflammatory process can be controlled. Our work shows how fish oils safely do this, and suggests a possible way to treating the serious problems of inflammation in obesity and in conditions like diabetes, cancer and cardiovascular disease through simple dietary supplementation."

However, Olefsky said more research is required. For example, it remains unclear how much fish oil constitutes a safe, effective dose. High consumption of fish oil has been linked to increased risk of bleeding and stroke in some people.

The effect of a 5-day fast on integrated, pulsatile, and periodic cortisol release was studied in 10 normal men by measuring serum cortisol concentrations every 20 min for 24 h before (day 0) and during the fifth day of fasting (day 5). Serum concentration profiles were analyzed for integrated cortisol release (area under the curve), pulsatile hormone release by an objective, statistically based pulse detection algorithm (cluster analysis), and periodic hormone release (circadian and ultradian rhythms) by Fourier expansion time series analysis. Urinary cortisol excretion per 24 h was measured in 5 men. The mean 24-h integrated serum cortisol concentration increased 1.7-fold during fasting (P = 0.0006). This increase resulted from a 2-fold increase in the serum cortisol concentrations between pulses (valley mean; P = 0.0004), an increase in the pulse height (P = 0.001), and an increase in pulse increment above baseline (P = 0.01). There were no changes in the number of pulses per 24 h, the interval between pulses, the width of the pulses, or the area of the pulses during fasting. Twenty-four-hour urinary cortisol excretion increased in all men, and the mean urinary cortisol (nanomoles per L)/creatinine clearance (milliliters per s) ratio increased from 119 on day 0 to 187 on day 5 (n = 5; P = 0.05). The pattern of periodic hormone release also changed during fasting; the mean (±SE) circadian rhythm (24-h) amplitude decreased from 160 ± 14 nmol/L on day 0 to 102 ± 105 nmol/L on day 5 (P = 0.06), and the amplitude of the 12-h rhythm increased from 68 ± 11 to 99 ± 11 nmol/L. There also were significant increases in the amplitudes of rhythms with periodicities of 8.1, 4.1, 2.4, 1.6, and 1.3 h (P = 0.02–0.008). Fasting in normal men results in distinct changes in the amount and pattern of pulsatile, circadian, and ultradian cortisol release.

Another study on fasting and cortisol, the stress hormone. Fasting makes you less stressed, eating glucose (bread, sugar), makes you more stressed, or stressable.

Center for Psychobiological and Psychosomatic Research University of Trier (C.K., N.R., C.G., K.M.P., D.H.H.), Trier, Germany; and Area of Psychobiology, Department of Psychology, University of Valencia (E.G.B., A.S.), Valencia, Spain

The availability of energy appears to exert important regulatory functions in pituitary-adrenal stress responses. In two studies, the effects of short-term fasting and subsequent glucose administration on the free cortisol response to psychological stress and nicotine consumption were investigated. Study 1: After fasting for 8–11 h, healthy young men ingested either 100 g glucose (n = 13) or water (n = 12). One hour later they were exposed to a psychosocial stress task (Trier Social Stress Test). A third group also ingested 100 g glucose, but they were not exposed to any additional treatment (n = 10). Capillary blood glucose levels were in the lower euglycemic range before and significantly elevated after the glucose load (64.9 ± 9.8 vs. 162.5 ± 43.5 mg/dL; F = 149.04, P < 0.001). Although glucose load per se did not affect free cortisol levels, psychosocial stress induced a large cortisol response in glucose-treated subjects. In contrast, fasted subjects who received tap water did not respond to the Trier Social Stress Test with significant changes in cortisol levels (F = 6.27, P < 0.001). Both groups responded with a similar increase in heart rates (F = 33.53, P < 0.001) with no statistically significant difference between glucose and water-treated subjects. Study 2: Twelve habitual smokers received 100 g glucose or tap water after fasting for at least 8 h on two separate sessions (cross-over, random sequence). Forty-five min after glucose/water ingestion, they smoked two cigarettes with a nicotine content of 1.0 mg/cigarette. Subjects were euglycemic before smoking, with a significant rise of glucose levels after consumption of 100 g glucose (64.4 ± 8.3 vs. 143.5 ± 40.0 mg/dL; F = 40.25, P < 0.001). As in Exp 1, subjects showed a substantially larger free cortisol response to nicotine under glucose load compared with water load (F = 4.91, P < 0.001).

From these data we conclude that the free cortisol response to stimulation is under significant control of centers responsible for monitoring energy availability. Low glucose levels appear to inhibit adrenocortical responsiveness in healthy subjects. In agreement with results from animal studies, the present results suggest that ready access to energy is a prerequisite for hypothalamus-pituitary-adrenal stress responses.

So consuming glucose makes your stress level go up faster. Look at all of us, eating carbs 3-5 times a day, and how stressed out we are. Recipe for road rage and stress overload.

Friday, October 22, 2010

Researchers at the University of California, San Diego School of Medicine have identified the molecular mechanism that makes omega-3 fatty acids so effective in reducing chronic inflammation and insulin resistance…Advertisement

The discovery could lead to development of a simple dietary remedy for many of the more than 23 million Americans suffering from diabetes and other conditions.

Macrophages are specialized white blood cells that engulf and digest cellular debris and pathogens. Part of this immune system response involves the macrophages secreting cytokines and other proteins that cause inflammation, a method for destroying cells and objects perceived to be harmful. Obese fat tissue contains lots of these macrophages producing lots of cytokines. The result can be chronic inflammation and rising insulin resistance in neighboring cells over-exposed to cytokines. Insulin resistance is the physical condition in which the natural hormone insulin becomes less effective at regulating blood sugar levels in the body, leading to myriad and often severe health problems, most notably Type 2 diabetes.

Fasting and stress have opposite influences on the energy expenditure of the human organism. The healthy human body is capable of passing from a state involving three regular food intakes to a state of short-term fasting and even prolonged fasting, as a result of precise metabolic regulation. In these cases, the organism will save as much energy as possible, thus reducing energy expenditure.

However, in stress conditions, energy expenditure is markedly increased. As a result, the body´s metabolism will be converted into a catabolic state, the gravity of which is determined by the nature and degree of the injury and type and severity of underlying disease.

These and other processes will be developed in the following chapters.

[Table of contents]

4.1 Effects of fasting

In theory, if a person having 15 kg of adipose triglycerides — i.e. 140.000 kcal of reserves in the form of fats (Cahill, 1970)— and energy requirements of 1800 kcal/day, begins to fast, he should be capable of withstanding 75 days of total fasting. In practice, an abstinence from feeding leads to death after about 50 days of total fasting. In other words, the theoretical value of the energy reserves can not be used in its entirety, because death intervenes beforehand due to partial depletion of functional tissue proteins.

In the case of abstinence or fasting, endogenous energy stores are used for metabolic processes. Fat, stored in indifferent fat tissue, is the major source of energy. Energy can also be derived from protein; however, there is no indifferent protein tissue and as a consequence the loss of protein always leads to a loss of organ function.

Hence, in the case of fasting in healthy persons, the metabolism is aimed at keeping the loss of protein as low as possible by lowering the metabolism and the gluconeogenesis. The loss of nitrogen is reduced in the case of complete fasting from 10 g per day to 4 - 5 g a day after 3 weeks. Fat stores are depleted faster with the purpose of providing energy.

Many organs including the heart, kidneys and muscles, can use either fatty acids or ketone bodies, derived from partial oxidation of fatty acids, directly as energy substrates. The central nervous system, on the other hand, and the red blood cells can only use glucose as an energy substrate. For example, during a 24 hour fast, the brain will consume 150 g of glucose and the other organs about 36 g, i.e. a total of 186 g of glucose per day. Since the body is incapable of synthesizing glucose from fat, it uses other substrates for gluconeogenesis. In fact, the glycogen reserves are insufficient to cover the requirements for more than 1 day. The most important substrate for gluconeogenesis is provided by amino acids and, to a minor extent, by glycerol derived from the triglycerides.Metabolism of short-term fastingFig. 8: Metabolism of short-term fasting

In short-term fasting, some of the glucose required by the brain is provided by liver glycogen, the reserve being exhausted within 48 hours. If the human body is to withstand fasting, it must mobilize 1800 kcal/day and produce 186 g of glucose mainly for the central nervous system. Eighty percent of the energy requirements are provided by lipolysis of adipose tissue where 160 g of triglycerides are split into fatty acids and glycerol. Approximately 75 g of muscle proteins, i.e. nearly 300 g of muscle, per day are mobilized to provide the substrate for gluconeogenesis. If protein breakdown were to continue at the initial rate, roughly one-third of the total body proteins would be exhausted in 3 weeks, which is incompatible with survival.

So, if fasting is prolonged, a major metabolic adaptation occurs. The central nervous system begins to use ketone bodies as an energy substrate, thereby reducing glucose requirements. Therefore, in prolonged fasting, there is a shift from the use of protein as an energy source towards the use of fats (in the form of ketone bodies). This adaptation permits protein sparing and preserves the proteins' functional role. Nevertheless, obligatory proteolysis always persists, amounting in the foregoing example to at least 20 g of protein daily.Metabolism of short-term fastingFig. 9: Metabolism of prolonged fasting

Metabolic processes respond to internal signals. During fasting, blood glucose levels fall with a consequent reduction in the secretion of insulin and an increase in glucagon, two hormones with antagonistic actions on energy metabolism. As a result of the decrease in the circulating insulin level, triglyceride catabolism increases, causing the release of free fatty acids and glycerol. The raised glucagon levels lead initially to a distinct increase in liver glycogenolysis. Further, gluconeogenesis is stimulated by glucagon, which inhibits protein synthesis and stimulates muscular proteolysis, thereby furnishing the amino acid substrate.

There is therefore a metabolic adaptation to prolonged fasting, resulting in a reduction of energy expenditure of up to 40% (Goldstein and Elwyn, 1989; Kinney, 1970). These mechanisms, which tend to limit proteolysis in the healthy person, are defective or non-operative in cases of severe disease or stress, as will be discussed in the next chapter.

Thursday, October 21, 2010

"On the occasion of World Heart Day (September 26) there’s a bad news for vegetarians Indians. As per a new research report presented by a Pune-based bariatric Dr. Shashank Shah, vegetarian Indians are more prone to suffer from heart ailments.

Commenting on why veggie Indians are more at risk of heart diseases, Dr. Shah said in a press statement, “We found that Indians are grossly deficient in vitamin B12, which is a crucial cardio-protective factor in the body.

Vitamin B12 is usually found in food that comes from animals, like fish, meat, poultry, milk and milk products. However, since a lot of Indians are vegetarians, they do not get adequate amounts of vitamin B12 in their diet.”"

[...]

Details of research studyTo come to this startling conclusion Dr Shah along with his colleague Dr Todkar, studied the data collected from about 300 patients from Hiranandani Hospital, Powai, over the period of one year.

They were startled to find out that 70 percent of these patients had suffered from a cardiac [pertaining to the heart.] disease or are at greater risk of cardiac attack in near future.

Nearly all of them were found to be suffering from vitamin B12 deficiency.

“When vitamin B12 levels fall, homocysteine levels increase. The latter is known to cause atherosclerosis (hardening and narrowing of the arteries), as well as an increased risk of heart attacks, strokes and blood clot formation,” noted Dr Shah in his study report.

1 From the Department of Nutrition, University of California, Davis, CA (DAM); INSERM ERI-12, UFR de Médecine et de Pharmacie, Université de Picardie Jules Verne, Amiens, France (TBD); and the Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA (EMS).

For the past 3 decades, the US government has promoted a policy of reduced dietary sodium intake as the principal nutritional means of reducing blood pressure and its attendant cardiovascular disorders in adults. Early on, this policy targeted at-risk individuals such as people with chronic arterial hypertension; however, in the past decade it has been applied to the population at large. Despite a litany of well-intended strategies from mandatory sodium labeling to extensive educational and social marketing efforts, there is little evidence that sodium intake has changed. In fact, some advocates of the policy have argued that sodium intake actually has increased, reaching extreme levels in some people (1). The failure of the government's efforts has been typically attributed to the food industry's excessive use of sodium in their products (1). Both the application of such a government policy to the entire population and the simplistic assessment that its failure to date can be attributed to the food industry's reluctance to provide lower sodium foods belie the scientific complexity of the issues, including sodium's role in health and disease.

In this issue of the Journal, Bernstein and Willett (2) provide a valuable analysis of 24-h urinary sodium (UNaV) data extracted from the medical literature published between 1957 and 2003. Their findings from the 38 US studies that met rigorous search criteria and involved 26,271 people confirm and extend the conclusions we published a year ago (3). Our analysis involved 19,151 people from 33 countries and 62 survey sites between 1984 and 2008. Like that of Bernstein and Willett, our analysis revealed a remarkably narrow range of UNaV across very diverse populations and eating habits, without the extreme levels often purported to exist by advocates of lower sodium intake (1) and no evidence of a change over time. The latter was best shown by the data of the UK Food Standards Agency between 1986 and 2008, which we noted (3) offered no evidence that an intense social marketing effort begun in 2005 had been successful.

One possible explanation, first raised by our report last year (3), is that human sodium intake is a parameter that even the most well intentioned public policy cannot modify in most people. An extensive body of basic science research, dating from Richter's seminal observations (4), has characterized an integrated network of peripheral hormonal signals interfaced with complex neural networks specific to regulating sodium intake of experimental animals (5). Although those basic research findings have not as yet been extrapolated to humans, they should not be completely ignored because they may yet provide a model of what is feasible in humans.

The current report extends our observations by documenting that, likewise, all the efforts in the United States over the past 3 decades have had no effect on the population's sodium intake. An alternative possibility for the stability of sodium intake is that sodium has been largely consumed in association with food intake, motivated by hunger and appetite. To the extent that caloric intake has been stable over populations and decades, so too has sodium. Thus, a potential benefit of reducing food sodium content would be a concurrent reduction of sodium. Working against that theoretical outcome, however, is the reality that over the millennia, before the introduction of processed foods, sodium was added to foods at the time of preservation, cooking, or consumption. An individual in our society has the identical options today as the food industry moves to offering more products whose ratio of calories to sodium is increased (ie, lower sodium content per serving). This individual choice could abrogate any effect on average sodium intake in society as these data indicate has happened.

Regardless of why sodium intake has been so stable, the data of Bernstein and Willett (2), as well those of McCarron et al (3), suggest that it is not a readily modifiable nutritional parameter for the population at large. Furthermore, a substantial body of research in humans provides evidence as to why this latest attempt to modify the general population's sodium intake is doomed to failure. Sodium has a critical role in extracellular fluid volume regulation as well as being of fundamental importance in cellular function across virtually all organ systems. Thus, it is unlikely that as an organism, humans would have evolved without the development of failsafe mechanisms to ensure sufficient sodium availability. Sodium is 1 of only 3 nutrients whose excretion in urine is recognized as regulated; water and glucose are the other 2. Consequently, deficits in these nutrients elicit immediate, potent, counterregulatory physiologic responses.

Low-fat diets have been shown to increase plasma concentrations of lipoprotein(a) [Lp(a)], a preferential lipoprotein carrier of oxidized phospholipids (OxPLs) in plasma, as well as small dense LDL particles. We sought to determine whether increases in plasma Lp(a) induced by a low-fat high-carbohydrate (LFHC) diet are related to changes in OxPL and LDL subclasses. We studied 63 healthy subjects after 4 weeks of consuming, in random order, a high-fat low-carbohydrate (HFLC) diet and a LFHC diet. Plasma concentrations of Lp(a) (P < 0.01), OxPL/apolipoprotein (apo)B (P < 0.005), and OxPL-apo(a) (P < 0.05) were significantly higher on the LFHC diet compared with the HFLC diet whereas LDL peak particle size was significantly smaller (P < 0.0001). Diet-induced changes in Lp(a) were strongly correlated with changes in OxPL/apoB (P < 0.0001). The increases in plasma Lp(a) levels after the LFHC diet were also correlated with decreases in medium LDL particles (P < 0.01) and increases in very small LDL particles (P < 0.05). These results demonstrate that induction of increased levels of Lp(a) by an LFHC diet is associated with increases in OxPLs and with changes in LDL subclass distribution that may reflect altered metabolism of Lp(a) particles.

Comment- Pretty straight up study, and low carb wins big time. Lipoprotein a, apo B, and oxidizzed phospolipids are all important markers of heart disease, and all of them got worse on low fat, better on low carb.